Donor cell-derived sarcoidosis after allogeneic BMT

Morita, Rena; Hashino, Satoshi; Kubota, Kanako; Onozawa, Masahiro; Kahata, Kaoru; Kondo, Takeshi; Suzuki, Shinya; Matsuno, Yoshihiro; Imamura, Masahiro; Asaka, Masahiro

doi:10.1038/bmt.2008.340

Cited by 10 publications

(13 citation statements)

References 5 publications

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“…The possibility of a transmissible agent was suggested for the development of sarcoidosis in the recipients in cases 1 and 2 [3,4]. However, there have been only two cases of donorderived sarcoidosis, which were confirmed by a chimerism analysis using their sarcoidosis lesions (case 9 [7] and the present case). The period from the HSCT in all of the reported cases, including the present case, was over 3 months (table 1).…”

mentioning

confidence: 49%

“…Three patients underwent autograft transplantation (cases 4-6) [5], and another three patients and the present case received stem cells from unrelated donors [6,7]. None of the donors in cases 3-9 or the present case had been diagnosed to have sarcoidosis before undergoing transplantation [5][6][7]. The possibility of a transmissible agent was suggested for the development of sarcoidosis in the recipients in cases 1 and 2 [3,4].…”

mentioning

confidence: 79%

“…In the present case and previously reported cases [3][4][5][6][7], the possibility of GVHD or a sarcoid reaction should be considered. Although chronic GVHD usually develops more than 3 months after transplantation, a series of findings suggestive of sarcoidosis in the present case appeared at 16 months after transplantation.…”

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confidence: 83%

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Sarcoidosis in donor-derived tissues after haematopoietic stem cell transplantation

et al. 2013

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confidence: 49%

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confidence: 79%

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Sarcoidosis in donor-derived tissues after haematopoietic stem cell transplantation

et al. 2013

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“…Case reports of sarcoidosis developing in bone marrow or solid organ transplant recipients suggest the existence of a transmissible agent or cell component in sarcoidosis [69][70][71][72]. Most commonly, sarcoidosis is discovered in donor solid organ allografts in recipients with a history of sarcoidosis [73][74][75][76][77][78][79][80], presumably inducing a granulomatous response by the recipient's immune system [81].…”

Section: Models Of Sarcoidosis Pathobiologymentioning

confidence: 99%

Etiologies of Sarcoidosis

Chen

Möller

2015

Clinic Rev Allerg Immunol

125

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Since sarcoidosis was first described more than a century ago, the etiologic determinants causing this disease remain uncertain. Studies suggest that genetic, host immunologic, and environmental factors interact together to cause sarcoidosis. Immunologic characteristics of sarcoidosis include non-caseating granulomas, enhanced local expression of T helper-1 (and often Th17) cytokines and chemokines, dysfunctional regulatory T-cell responses, dysregulated Toll-like receptor signaling, and oligoclonal expansion of CD4+ T cells consistent with chronic antigenic stimulation. Multiple environmental agents have been suggested to cause sarcoidosis. Studies from several groups implicate mycobacterial or propionibacterial organisms in the etiology of sarcoidosis based on tissue analyses and immunologic responses in sarcoidosis patients. Despite these studies, there is no consensus on the nature of a microbial pathogenesis of sarcoidosis. Some groups postulate sarcoidosis is caused by an active viable replicating infection while other groups contend there is no clinical, pathologic, or microbiologic evidence for such a pathogenic mechanism. The authors posit a novel hypothesis that proposes that sarcoidosis is triggered by a hyperimmune Th1 response to pathogenic microbial and tissue antigens associated with the aberrant aggregation of serum amyloid A within granulomas, which promotes progressive chronic granulomatous inflammation in the absence of ongoing infection.

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“…Reports of granulomatous inflammation developing after receiving bone marrow or solid organ transplants from donors with sarcoidosis have suggested this is the result of a transmissible agent in sarcoidosis. [60][61][62][63] One report suggests that these events may reflect the immunogenetics of the donor MHC haplotypes being associated with an increased risk of developing sarcoidosis. 64 The development of granulomatous inflammation in donor allografts following lung, heart, liver, and kidney transplantation into recipients with sarcoidosis also suggests that the responsible agents for sarcoidosis may be transmittable.…”

Section: Transplantation Insightsmentioning

confidence: 99%

Etiologic Role of Infectious Agents

Chen

Möller

2014

Semin Respir Crit Care Med

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A consensus statement found in most peer-reviewed literature on sarcoidosis is that the etiology of sarcoidosis is unknown. It is timely to review whether this statement should be revised. Many infectious agents meet the basic requirements of inducing granulomatous inflammation and immunologic responses consistent with sarcoidosis including oligoclonal expansion of CD4+ T cells, polarized Th1 and possibly Th17 responses, and dysregulated regulatory T-cell function. Studies over the past decade provide increasing and complementary data to implicate a role for infectious agents in sarcoidosis etiology. These studies used different methodologies such as polymerase chain reaction and mass spectrometry to document microbial nucleic acids and proteins in sarcoidosis tissues. Multiple studies report antigen-specific immune responses to specific microbial proteins in sarcoidosis. In aggregate, these studies provide compelling evidence that mycobacteria play a major etiologic role in sarcoidosis in the United States and Europe. Studies from Japan support a role for Propionibacteria as a major etiologic agent in the country. There is controversy over how these (or other) infectious agents cause sarcoidosis. The hypothesis that chronic sarcoidosis is caused by a viable, replicating mycobacterial or other infection has no direct pathologic, microbiologic, or clinical evidence. A novel hypothesis links microbial triggers to a sarcoidosis outcome from the accumulation of aggregated proinflammatory serum amyloid A within granulomas, providing a mechanism for chronic disease in the absence of any viable tissue infection. Further studies are needed to provide more definitive evidence for these competing hypotheses before the statement that the etiology of sarcoidosis is unknown becomes obsolete.

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Donor cell-derived sarcoidosis after allogeneic BMT

Cited by 10 publications

References 5 publications

Sarcoidosis in donor-derived tissues after haematopoietic stem cell transplantation

Sarcoidosis in donor-derived tissues after haematopoietic stem cell transplantation

Etiologies of Sarcoidosis

Etiologic Role of Infectious Agents

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